ArticleJournal of virology2020
An Animal Model That Mimics Human Herpesvirus 6B Pathogenesis.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Review
- A viral APOBEC3 antagonist distinguishes HHV-6A from HHV-6B.Nature communications · 2026Article
- Update on human herpesvirus 7 pathogenesis and clinical aspects as a roadmap for future research.Journal of virology · 2024Review
- ATF1 Restricts Human Herpesvirus 6A Replication via Beta Interferon Induction.Journal of virology · 2022Article
- Disruption of thymic central tolerance by infection with murine roseolovirus induces autoimmune gastritis.The Journal of experimental medicine · 2022Article
- Murine roseolovirus does not accelerate amyloid-β pathology and human roseoloviruses are not over-represented in Alzheimer disease brains.Molecular neurodegeneration · 2022Article
- Human Herpesvirus 6A Tegument Protein U14 Induces NF-κB Signaling by Interacting with p65.Journal of virology · 2021Article
- Tetrameric glycoprotein complex gH/gL/gQ1/gQ2 is a promising vaccine candidate for human herpesvirus 6B.PLoS pathogens · 2020Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human herpesvirus 6B (HHV-6B), a T-lymphotropic virus, infects almost exclusively humans. An animal model of HHV-6B has not been available. Here, we report the first animal model to mimic HHV-6B pathogenesis; the model is based on humanized mice in which human immune cells were engrafted and maintained. For HHV-6B replication, adequate human T-cell activation (which becomes susceptible to HHV-6B) is necessary in this murine model. Here, we found that an additional transfer of human mononuclear cells to humanized mice resulted in an explosive proliferation of human activated T cells, which could be representative of graft-versus-host disease (GVHD) because the primary transfer of human cells was not sufficient to increase the number and ratio of human T cells. Mice infected with HHV-6B became weak and/or died approximately 7 to 14 days later. Quantitative PCR analysis revealed that the spleen and lungs were the major sites of HHV-6B replication in this model, and this was corroborated by the detection of viral proteins in these organs. Histological analysis also revealed the presence of megakaryocytes, indicating HHV-6B infection. Multiplex analysis of cytokines/chemokines in sera from the infected mice showed secretions of human cytokines/chemokines as reported for both
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